Exploring the relationship between MGAT2 and glioblastoma: A Mendelian Randomization and bioinformatics approach

Mannosyl-glycoprotein beta-1,2-N-acetylglucosaminyltransferase 2 (MGAT2) and tumors' relevant research was in full swing recently. Therefore, we employed Mendelian Randomization (MR) alongside bioinformatics to thoroughly investigate the possible relationship between MGAT2 and glioblastoma (GBM).

We utilized the summary statistics of genome-wide association studies (GWAS) for MGAT2 (N = 35,559 from deCODE) and glioblastoma (N = 379,155 from FinnGen). MR was used to assess the causal relationship between MGAT2 and GBM. Bioinformatics was used for a more in-depth exploration of the relationship between MGAT2 and GBM.

MR analysis demonstrated a causal relationship, showing that elevated levels of MGAT2 are associated with an increased risk of GBM (OR = 2.59, 95 % CI: 1.13-5.91, p = 0.023). Further investigation revealed significant differences in MGAT2 expression across normal tissue, tumor tissue, and gliomas of different types. Additionally, we found that MGAT2 may influence GBM through immune-related pathways, particularly through the role of macrophages. Proteins associated with MGAT2 were also identified in the PPI network.

This study first validated the causal relationship between MGAT2 and glioblastoma, and used bioinformatics to explore the relationship from multiple perspectives. Additionally, we proposed hypotheses for further research to investigate the potential mechanisms underlying this connection.